title: Effect of acidotic blood reperfusion on reperfusion injury after coronary artery occlusion in the dog heart.
abstract: A prolongation of the intracellular acidosis after myocardial ischemia can protect the myocardium against reperfusion injury. In isolated hearts, this was achieved by prolongation of the extracellular acidosis. The aim of this study was to investigate whether regional reperfusion with acidotic blood after coronary artery occlusion can reduce infarct size and improve myocardial function in vivo. Anesthetized open-chest dogs were instrumented for measurement of regional myocardial function, assessed by sonomicrometry as systolic wall thickening (sWT). Infarct size was determined by triphenyltetrazolium staining after 3 h of reperfusion. The left anterior descending coronary artery (LAD) was perfused through a bypass from the left carotid artery. The animals underwent 1 h of LAD occlusion and subsequent bypass-reperfusion with normal blood (control, n = 6) or blood equilibrated to pH = 6.8 by using 0.1 mM HCl during the first 30 min of reperfusion (HCl, n = 5). Regional collateral blood flow (RCBF) at 30-min occlusion was measured by using colored microspheres. There was no difference in recovery of sWT in the LAD-perfused area between the two groups at the end of the experiments [-2.8+/-1.2% (HCl) vs. -4.4+/-2.5% (control); mean +/- SEM; p = NS]. RCBF was comparable in both groups. Infarct size (percentage of area at risk) was reduced in the treatment group (12.8+/-2.8%) compared with the control group (26.2+/-4.8%; p < 0.05). These results indicate that reperfusion injury after coronary artery occlusion can be reduced by a prolonged local extracellular acidosis in vivo.
authors.affiliation: Physiologisches Institut I, Abteilung für Herz- und Kreislauf-Physiologie, Heinrich-Heine-Universität Düsseldorf, Germany.
authors.forename: B
authors.initials: B
authors.lastname: Preckel
authors.forename: W
authors.initials: W
authors.lastname: Schlack
authors.forename: D
authors.initials: D
authors.lastname: Obal
authors.forename: H
authors.initials: H
authors.lastname: Barthel
authors.forename: D
authors.initials: D
authors.lastname: Ebel
authors.forename: S
authors.initials: S
authors.lastname: Grunert
authors.forename: V
authors.initials: V
authors.lastname: Thämer
mesh_terms: D000138:Acidosis / Q000097:blood; D000818:Animals; D003326:Coronary Circulation; D004285:Dogs; D005260:Female; D006321:Heart / Q000033:anatomy & histology; D006439:Hemodynamics; D006851:Hydrochloric Acid / Q000097:blood; D006863:Hydrogen-Ion Concentration; D008297:Male; D009203:Myocardial Infarction / Q000473:pathology; D017202:Myocardial Ischemia / Q000503:physiopathology / Q000628:therapy*; D015428:Myocardial Reperfusion Injury / Q000000981:diagnostic imaging / Q000517:prevention & control*; D009929:Organ Size; D014463:Ultrasonography; D016277:Ventricular Function, Left
chemical_list: D006851:Hydrochloric Acid